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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Diabetes-induced changes in responsiveness of rat bladder and vas deferens to peptides in vitro: susceptibility to reversal by insulin.
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Diabetes-induced changes in responsiveness of rat bladder and vas deferens to peptides in vitro: susceptibility to reversal by insulin.

机译：糖尿病引起的大鼠膀胱和输精管对肽的体外反应性变化：胰岛素逆转的敏感性。

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Changes in responsiveness of the vas deferens and urinary bladder to bradykinin (BK) receptor agonists (Tyr8-BK and des-Arg9-BK), substance P (SP), and endothelin-1 (ET-1) were assessed 8 weeks after streptozotocin (STZ)-induced diabetes. Preparations from control or STZ-treated (60 mg/kg i.p.) male rats were tested for contractile and neurogenic twitch potentiating (TP, in VD only) effects of all four agonists (1 nM to 0.3 or 3 microM). In diabetic VD, contractile effects of Tyr8-BK, des-Arg9-BK, and SP were enhanced, but ET-1 effects were unchanged. In contrast, TP by des-Arg9-BK was unaffected, that by Tyr8-BK was decreased, and those by SP and ET-1 were increased. In diabetic UB, only contractions to des-Arg9-BK and SP were enhanced. Following insulin replacement (human, 1-3 U/day s.c.), starting 1 week after STZ, TP induced by Tyr8-BK and des-Arg9-BK in VD were further inhibited, but all other changes in both preparations were reversed at least partially. Insulin treatment of nondiabetic rats, however, also affected VD (but not UB) responsiveness, such that contractions to Tyr8-BK and TP by ET-1 were increased, but TP by Tyr8-BK was decreased. Thus, STZ-induced type I diabetes causes important alterations in responsiveness of non-vascular smooth muscle tissues of the rat to BK, SP, and ET-1. Long term insulin replacement, at doses normalising glycaemia, effectively reversed most changes in VD or UB responsiveness, but it is unclear if this is truly due to blocking of STZ-induced changes, since the treatment also affected responsiveness of nondiabetic tissues.
机译：在链脲佐菌素治疗8周后评估输精管和膀胱对缓激肽（BK）受体激动剂（Tyr8-BK和des-Arg9-BK），P物质（SP）和内皮素-1（ET-1）的反应性变化。 （STZ）诱发的糖尿病。测试来自对照或经STZ处理（60 mg / kg腹膜内）的雄性大鼠的制剂对所有四种激动剂（1 nM至0.3或3 microM）的收缩和神经源性抽搐增强作用（TP，仅在VD中）。在糖尿病性VD中，Tyr8-BK，des-Arg9-BK和SP的收缩作用增强，但ET-1的作用不变。相反，des-Arg9-BK的TP不受影响，Tyr8-BK的TP降低，而SP和ET-1的TP升高。在糖尿病UB中，仅对des-Arg9-BK和SP的收缩增强。更换胰岛素后（人，每天1-3 U /天），从STZ后1周开始，进一步抑制了Vyr中Tyr8-BK和des-Arg9-BK诱导的TP，但是两种制剂中的所有其他变化至少都被逆转了部分地。然而，非糖尿病大鼠的胰岛素治疗也影响了VD（但不影响UB）的反应性，因此ET-1对Tyr8-BK和TP的收缩增加，而Tyr8-BK的TP降低。因此，STZ诱导的I型糖尿病会导致大鼠非血管平滑肌组织对BK，SP和ET-1的反应性发生重要变化。长期使用胰岛素使血糖正常化，可以有效逆转大多数VD或UB反应性变化，但是尚不清楚这是否真的是由于STZ诱导的变化受阻，因为治疗还影响了非糖尿病组织的反应性。

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